We have shown that binocular input to neurons of the visual cortex of cats monocularly deprived of vision from birth can be restored by both the intravenous and the microiontophoretic administration of bicuculline, an antagonist of the inhibitory neurotransmitter GABA. We hypothesize that the deficits produced by this experimental analogue of amblyopia are mediated, at least in part, by excessive and asymmetrical inhibition. Naloxone, a clinically used anti-opiate also with anti-GABA actions, similarly restores binocularity in monocularly deprived cats. Many deprived eye receptive fields appear to have normal characteristics. Thus, the ability to reverse the deficits of deprivation amblyopia has not only theoretical but clinical implications as well. We plan: (1) to study the effects of disinhibition upon neurophysiological correlates of amblyopic visual acuity loss; (2) to determine whether disinhibition improves functional visual acuity; (3) to search for longer acting and less toxic disinhibitors; (4) to contrast and compare pharmacological disinhibition with that produced by enucleation of the normal eye; (5) to develop a new, more clinically relevant, and deprivation-free model of amblyopia; (6) to determine the necessary and sufficient conditions for the development of amblyopia, especially to examine the role played by pattern deprivation and selective visual attention; and (7) to synthesize a rational approach to clinical amblyopia and related disorders based upon experimental findings.